Acromegaly
Conditions
Brief summary
Since protein and AAs are master regulator of GH and IGF-I secretion, we hypothesized that a low protein diet could reduce GH and IGF-I levels in acromegalic patients in addition to conventional therapy. Furthermore, we aim to explore metabolomic, microbiota, and micro-vesicle fingerprints of GH hypersecretion during conventional therapy and after a low protein diet
Detailed description
Nutrients are crucial modifiers of the GH/IGF-I axis. In particular, a close cross-talk between proteins and amino acids (AAs) and GH/IGF-I secretion exists. Both AAs and proteins affect GH secretion. AAs stimulate GH secretion upon oral administration, with different potency among studies, being the combination of arginine and lysine the most powerful. Soy proteins also stimulate GH secretion when ingested either as hydrolysed proteins or free AAs. Furthermore, the acute GH response to AAs ingestion may be influenced by the daily amount of dietary protein/AAs consumption: diets high in proteins apparently increase basal GH levels. AAs and proteins have a positive effect on IGF-I secretion as well. In general, high levels of proteins, especially animal and dairy proteins, and consumption of branched chain amino acids (BCAAs) increase serum IGF-I levels. Considering pathological GH conditions, metabolomic analysis of acromegalic patients suggests that the main metabolic fingerprint of GH hypersecretion is a reduction in BCAAs, related to the disease activity. Moreover, there is evidence that GH, rather than IGF-I, is the main mediator of such metabolic fingerprint, which may be related to increased uptake of BCAAs by the muscles, increased gluconeogenesis, and raised consumption of BCAAs. Thus, in acromegaly, a tailored diet is a further strategy that may contribute to blunt GH/IGF-I secretion. Indeed, some authors recently suggested that personalized or precision nutrition in some conditions and diseases could have an impact on their phenotype, combining dietary recommendations with individual's genetic makeup, metabolic and microbiome characteristics, and environment. However, studies on precision nutrition in acromegaly are still in a neonatal era.
Interventions
OTHERUsual clinical practice + hypoproteic diet
Diet will be composed by: * energy equal to daily energy expenditure (estimated by indirect calorimetry \* physical activity factor) * fats 28-35% * carbohydrates 50-60% * proteins 0,7-0,8g/kg of body weight 10-13% Diet will be given to the patient after the first visit and the study will start once the patient begins the diet.
Sponsors
Azienda Ospedaliero Universitaria Maggiore della Carita
Study design
Allocation
NA
Intervention model
SINGLE_GROUP
Primary purpose
TREATMENT
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
18 Years to 65 Years
Healthy volunteers
No
Inclusion criteria
* Age 18/65 * Diagnosis of Acromegaly * In therapy with somatostatin analogues
Exclusion criteria
* pregnancy or lactation * alchool or drugs abuse * cancer * Hematological diseases
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Change in disease related hormones | Change from Baseline GH, IGF-1, IGFBP1, IGFBP3 blood levels at 15 days, 30 days, 45 days, 60 days | Variation of GH, IGF-1, IGFBP1, IGFBP3 hormones |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Change in body circumferences | Change from Baseline circumferences at 15 days, 30 days, 45 dyas, 60 days | Variation of body circumferences (waist, hips) |
| Change in metabolic control | Change from Baseline lipid profile at 15 days, 30 days, 45 days, 60 days | Change of cardio-metabolic risk factors: lipid profile |
| Change in kidney profile | Change from Baseline Serum Creatinin at 15 days, 30 days, 45 days, 60 days | Variation of serum creatinin |
| Change in liver profile | Change from Baseline Serum Creatinin at 15 days, 30 days, 45 days, 60 days | Variation of liver markers(AST, ALT, GGT) |
| Change in uric acid | Change from Baseline uric acid in blood at 15 days, 30 days, 45 days, 60 days | Variation of uric acid in blood through enzymatic determination |
| Change in weight | Change from Baseline BMI at 15 days, 30 days, 45 days, 60 days | Variation of body weight assessed through body mass index change (BMI)(kg/m2) |
| Change in blood count | Change from Baseline blood count at 15 days, 30 days, 45 days, 60 days | Variation of blood count |
| Change in microbiota | Change from Baseline of prevalence of microbiota phyla at 15, 30 days, 45 days, 60 days | Variation of prevalence of microbiota phyla through DNA sequencing of stools |
| Change in omics profile | Change from Baseline omic profile of stools at 15, 30 days, 45 days, 60 days | Variation of lipidomic profile of stools through liquid and gas chromatography |
| Change in microvesicles | Change from Baseline microvesicles levels at 15, 30 days, 45 days, 60 days | Variation of urinary microvesicles levels |
| Change in basal metabolic rate | Change from Baseline basal metabolic rate at 60 days | Variation of basal metabolic rate (kcal) |
| Change in body composition | Change from Baseline fat mass% at 60 days | Change of body composition (fat mass %) (BIVA) |
Countries
Italy
Outcome results
None listed